If you’ve ever seen someone with a baby, chances are you’ve heard them say something along the lines of “You’re so cute; I could just eat you up!”

Well a recent article published in Frontiers in Psychology by a research team at the Technische Universität of Dresden, Germany shows there may be a link between an infant’s smell and a female’s response, depending on the status of the female. Scientists have studied the connection between olfactory signals and the bond between a mother and her infant in several non-human mammal species. However, up until now, the research performed on mother-infant bonding in humans has only ever explored the visual and auditory senses.

What they did:
A total of 30 women were tested. Fifteen of the women had given birth for the first time three to six weeks prior to the experiment (primiparous). The other 15 women had never given birth (nulliparous). To obtain the sample odors, 18 infants each wore a T-shirt for two nights postpartum. The shirts were then placed in plastic bags and frozen to keep the odor unaltered. During the experiment, each woman was exposed to both “odorless” air and the odors of two different infants; primiparous women were never exposed to their own baby’s odor. The women were asked to rate the odor on intensity, familiarity, and pleasantness, though none of the participants were aware of what the odor stimulus was. As the women processed the different odors, an fMRI machine scanned their brain.

What they found:
Overall the women rated the infant odors as “weak, unfamiliar, and mildly pleasant”. The researchers found no significant difference in the overall ratings of intensity, familiarity, and pleasantness between the primiparous women and the nulliparous women. Despite the relatively “weak” rating of the odor, they did however find a difference in brain activity. The caudate nucleus of the primiparous women were significantly more responsive to the neonatal odors than those of nulliparous women. When compared to the responses of “odorless air,” the nulliparous women did show increased activity in the caudate nucleus, indicating that the neonatal odors trigger an effect (though not as great) in females who aren’t mothers. The definite contrast between the two groups, suggests that the effects are dependent on the status of the female.

The caudate nucleus, of which dopamine is the chief neurotransmitter, has already been linked to reward learning mechanisms. Through dopaminergic pathways, our bodies can learn to associate certain behaviors with a positive feeling, prompting us to act in a certain way. In this case, females are motivated to show motherly behavior because these actions have been associated with pleasure. The same “circuit makes us desire certain foods and causes addiction to tobacco and other drugs,” says postdoctoral researcher and lecturer at the University of Montreal, Johannes Frasnelli. “Not all odors trigger this reaction. Only those associated with reward, such as food or satisfying a desire, cause this activation.”

The research on this topic is just getting started. This experiment left several questions unanswered, such as what effect do neonatal odors have on males? There also wasn’t any control odor that triggered the same response as the neonatal odors, so the direct link to reward mechanisms needs to be further researched. However, previous studies have shown similar brain activation in the responses of women looking at baby faces. The fact is that babies rely on these behavioral effects for survival.

Babies can’t care for themselves, and when you think about babies objectively, they don’t do much. They eat. They sleep. They cry. They poop. And yet, sleep deprived mothers continue to care for, nurture, and protect their babies. And much of it has to do with the seemingly inexplicable mother-child bond that teaches the body to reward these affectionate parental behaviors with a pleasurable sensation. So it makes sense that the satisfaction a hungry teenager gets from devouring an entire pizza is equal to that of a mother caring for her baby. Since these sensations both work along dopaminergic pathways it’s no wonder we sometimes think babies smell good enough to eat. Luckily for us these are only ephemeral sensations that we thankfully can resist. Otherwise, well, some of us might not be here…

]]>http://sites.bu.edu/ombs/2013/10/02/mothers-eating-their-babies-no-its-not-cannibalism/feed/0Cupidity of Commodityhttp://sites.bu.edu/ombs/2013/09/24/cupidity-of-commodity/
http://sites.bu.edu/ombs/2013/09/24/cupidity-of-commodity/#commentsTue, 24 Sep 2013 23:59:07 +0000Matthew Jahnkehttp://sites.bu.edu/ombs/?p=6055WARNING: the following article features sentences written either by professionals or under the supervision of professionals. Accordingly, Matt and the producers must insist that no one attempt to recreate or re-enact any sentence or thought described in this article.

Personal Note from the Producers: Don’t feed into the character Matt creates, he truly is a good person. #NWTS

Cue the Pink Floyd…

Boom boom ba boom boom boom ching ching guitar riff….”MONEY!”

What do you want? What do you need? Food? Water? Shelter? Sure, sure, yes maybe, but what do you want? Dream bigger, you’re thinking too realistically! Stop limiting yourself, open up! Close your eyes, relax, paint the picture how you see it. Don’t tell me, just visualize it, taste it, feel it! C’mon man, it’s in there somewhere! Yes Yes, exactly bottle up all those ‘it’s not gonna happen’ or ‘yeah right’ moments you experienced and strangle the life out of them! You want the Arancio Argos Lamborghini Aventador LP 700-4 with the matte wheels to match, okay. You liked that bachelor pad in Phuket didn’t you? The one with the wrap around balcony, snug love seat, black leather couch, gourmet kitchen, his/her bathrooms…yeah that’s the one. But how? That’s impossible right? How do you expect to reward yourself with such prodigal riches at such a young age? Who are you trying to follow? Me: Floyd “Money” Mayweather, Adrien Broner, Scott Disick, Lavish P! Because we’re all rich peasants! If you can’t afford to roll with the crew baby, then you’re merely a campesino (shout out to to the Spanish readers). We get everything we want! There ain’t no morality in this [bleep]! We might as well call ourselves the seven deadly sins! We take pride in our beliefs, feed off of your envy, consume more than we require, lust in the beauty of those we surround ourselves with, avoid physical labor, laugh at your anger, and most importantly: ignore the realm of the spiritual because its not worth a dime! Now, I love me some greed in the morning, especially served with a bowl of lucky charms. But is the idea of greed more innate than we think it is? Are the moral perceptions of greed and neuroscience more intertwined than we think? Shall we…

Barclays chief executive Bob Diamond once said that the best test of responsible banking is to know “how people behave while no one is looking.” Senior bankers are among the first individuals to be consumed by greed. Granted enormous amounts of ‘superpower’ if you will, these men often succumb to the brain-changing effects of prosperity which results in distorted forms of behavior, emotions, and associated feelings. But bankers are not the only ones to fault here. In any case, an added boost of testosterone increases the chemical messenger’s release of dopamine in the brain’s reward systems. Combine excessive power + additional testosterone + dopamine to essentially justify ones actions and you have a recipe for an egocentric, un-empathetic pig. But how can we measure the obsessive pursuit of rewards — financial, interpersonal, material, sexual — and likelihood to treat others as objects with a dulled perception of risk? By analyzing the neural ‘approach mode’ that focuses on the biases of attention, memory, actions, and emotions geared towards reward and conquest, we can identify which chemical messenger systems are responsible for the corresponding impulse. One study at Texas A&M University, for example, is analyzing these impulses to determine if their is an associated correlation between men’s willingness to cheat on women to fulfill the temptation created by this rush of chemicals. To better understand the chemical reward systems we’re looking at, let’s dive into the mesolimbic dopamine system.

Associated dopamine pathways reduce stress and reward behavior

Specifically, the VTA-NAc circuit is the key to understanding the impulse of a reward stimulus. Under normal conditions, the circuit controls an individuals responses to basic rewards, such as food, water, and social interaction; therefore, an important moderator of motivation and drives. Additionally, the activation of this circuitry reinforces the individuals actions so as to repeat what was necessary to receive the reward. In essence, if a behavior can be successfully attributed to obtaining a particular reward, a rush of dopamine through the medial forebrain bundle will reinforce these actions in order to repeat the process. The flaw of this biological system comes down to the behavior itself. When behavior that might classify as ‘greed’ falls into this cycle, while varying greatly, the downward spiral can truly begin. While mild forms of greed can be an unwillingness to give a dollar to a homeless person, more severe examples can be seen via our senior bankers, who are capable of skimming off millions of dollars for further investment in adultery, fast cars, and other personal assets. But is greed simply a matter of falling into a self-induced mesmeric focus on personal gain without risk? Kind of, but mental modes are more complex than that. For example, a depressed person may have greater difficulty recalling a positive experience while those with a more ‘buoyant’ mode of thinking may have greater difficulty recalling a negative experience. Research being done at Tilburg University is looking into the effect power flux has on these mental modes. Studies have currently shown that individuals with increased power and avarice often lack sympathy towards others and can be hypercritical despite their judgments being self-applicable. Coupled with increased unethical tendencies in decision-making its no wonder why such individuals are disliked by your average person.

If you’re unaware of ‘Lavish P.,’ I would start there. He’d be your first rate example of what greed might be. I’m not firing shots at him or his twitter account because personally, I do find him interesting. Flaunting Louis Vuitton as his favorite brand and dropping his recent single “I Get Everything I Want” on Youtube, Lavish isn’t shy when it comes to showing what he has. He’s not afraid to take shots at celebrities, not afraid to give away money to the “peasants” that are beneath him (AKA everyone?) , and not afraid to stand by the persona he’s created, which is at least admirable. But does he fit the mold? Who knows? In fact, nobody except Lavish knows whether or not he’s created a remarkable publicity stunt through social media or he was just born this way. I guess if I’m the next peasant in line to receive $100,000 from him, I won’t complain. But for now, I’ll admire from afar, keeping my expectations of my future assets in perspective, while aspiring to fulfill my dreams at the same time because at the end of the day, isn’t that why we’re here?

Lobsters, Axons, Telephones, and Extracellular Recordings – A look at how neuronal signals can be transmitted differently under certain pharmacological conditions.

Neuronal signals are normally transmitted from cell bodies, or somas, to terminals via extensions called axons. At these terminals, connections called synapses are made with other neurons whereby the signals are released via the aide of chemical messengers called neurotransmitters. Many still believe that axons are reliable conductors of these signals.

However, with several years’ worth of experiments, scientists have questioned the fidelity of axonal conduction. They’ve realized that axons do not work like telephones. While telephones and axons may both have buttons – at the terminals in axons – only telephones faithfully conduct signals. And only telephones ring aloud and send messages to voicemail…

In any case, neuronal signals, unlike telephone signals, can change along their paths. Moreover, the pre-synaptic neuron may communicate a different message from the one originally sent from the soma to the synapse with the post-synaptic cell. Researchers at the lab I’ve been working at this summer, the Whitney Laboratory for Marine Bioscience, have focused on the role of neuromodulation in signal transmission along axons, particularly by the well-known neurotransmitter – dopamine.

Top Left, Homarus americanus. Bottom Left, Nervous system pinned down for recordings. Right, Recordings in vivo and in vitro.

Dissecting out the stomatogastric nervous system of the Homarus americanus, or Maine Lobster, Dirk Bucher, Aleksander Ballo, and colleagues have been able to take extracellular – and intracellular – recordings from axons. Using these recordings, they focus on how signal transmission differs under control and pharmacologically affected conditions.

Bucher and Ballo are some of the first researchers to directly show that neuromodulators affect activation properties of axonal voltage-gated ion channels – particularly looking at HCN channels. First off, these channels carry the hyperpolarization-activated inward current, which brings positive ions into the axon and initiates depolarization. Secondly, researchers including Ballo and Bucher suggest these channels influence neuronal communication by affecting the timing and efficacy of spikes and bursts. Further, they suggest the channels balance positive and negative currents to improve fidelity when there is repetitive spiking; this type of spiking can occur through many central pattern generators, such as those involved in rhythmic behaviors like walking, chewing, and swimming.

Spikes can also be initiated peripherally by dopamine administration. Ballo and Bucher offer that dopamine acts through D1-type receptors to increase cAMP which then works to modulate HCN channels.

Second messenger mechanism by which dopamine increases cAMP to influence HCN channels and corresponding currents

Often this series of events increases axonal conductance. When the current at these HCN channels is blocked, dopamine has no effect, suggesting also its importance in fidelity of axonal conduction.

Hopefully with more research into how signals can be altered after production at the soma, we can better understand how rhythmic behaviors are initiated, maintained, and restored.

Going on vacation with my family for thirteen days was both exciting and daunting. The West Coast adventure was extremely appealing and I couldn’t wait to see the Grand Canyon, explore Yosemite National Park, and drive a convertible down the Pacific Coast Highway. But where was I going to get my brain fix? The Scientific American issue I bought for the flight to Phoenix wasn’t doing it for me. Some hope was gained at The Exploratorium, a hands-on science museum in San Francisco that managed to convince my thirteen-year-old sister that neuroscience might be almost potentially cool, but it wasn’t until a trip to Sonoma County that my curiosity was finally piqued.

Tiger the horse and I were riding along on a vineyard tour and I was talking to the tour guide about school. I’ve got yet another new response to “I’m studying neuroscience”: the tour guide told me about his son’s mysterious mental illness that may or may not be schizophrenia and we rode through wine country discussing psychiatrists, Thorazine, thought disorders and SSRIs. All in all, a good day.

This conversation got me wondering about the kinds of challenges psychologists and psychiatrists face when having to diagnose patients with schizophrenia. All the clinicians have to go on are whatever behavioral abnormalities make themselves apparent. But how do you weed out schizophrenia from other kinds of psychosis (some of which may respond to the typical treatment for schizophrenia)?

In March, scientists in Finland published a paper in Genome Medicine in which they described a study done on patients with DSM-IV primary psychosis – disorders that included schizophrenia, other non-affective psychosis (ONAP) and affective psychosis. The researchers measured cholesterol (HDL and LDL), triglycerides, glucose, insulin, C-reactive protein (CRP) and cotinine. They also measured blood pressure, weight, and waist circumference as well as asking for the participants’ use of butter versus vegetable oil, fat content in milk products, and use of raw vegetables. The study investigated various metabolic processes that could be associated with schizophrenia, with the hope that certain metabolites have the potential for use as diagnostic tests for the disorder.

Schizophrenics tend to have a high level of fasting total triglycerides and show insulin resistance, but this feature is usually seen as a side effect of antipsychotic medication. However, other recent studies have shown abnormal insulin secretion and glucose response, along with diabetes risk, to be common in new schizophrenia patients who have yet to start treatment. One study, published in Molecular Psychiatry last year, showed that despite normal to slightly elevated glucose levels, untreated schizophrenia patients showed heightened levels of insulin and related proteins (the precursor proinsulin, the intermediate des31,32-proinsulin, C-peptide, which links the A and B chains of insulin, and chromogranin A, a precursor to other secretory hormones) where their bipolar counterparts did not. The extra insulin could certainly have a negative effect on brain function.

In the Genome Medicine study, branched-chain amino acids (BCAAs) from metabolic cluster MC3 were elevated in the schizophrenia patients. BCAAs are important to insulin secretion and they also compete with aromatic amino acids trying to cross the blood-brain barrier, suggesting a possible mechanism for psychosis. A drop in concentration of the amino acids needed to make catecholamines and serotonin in the brain (tyrosine and tryptophan, respectively) could be part of the problem. Perhaps this is why the tour guide’s son had spent some time on SSRIs when a clinician thought he was schizophrenic – although the drugs didn’t do much for his problem.

Catecholamines and serotonin don’t make up the whole story, which could have been why the SSRIs didn’t help this young man’s illness even if he definitely had schizophrenia. Another pathway that this article links to the schizophrenia mystery involves the up-regulation of proline that is apparent in schizophrenia patients. Many patients seem to be predisposed to variations of the PRODH gene that cause a decrease in proline oxidase. The result (excess proline in the brain) has been associated with cognitive dysfunction.

Too much proline and too much insulin, BCAAs competing with tyrosine and tryptophan – I’d never read this before, and my tour guide told me that his son was doing well on Thorazine, a drug (as I’d learned in school) was used to put the brakes on dopamine in patients with which disorder? Schizophrenia.

What about dopamine, then? It turns out that the hypothesis relating overabundance of dopamine to schizophrenia is somewhat outdated. Studies have shown that patients who did not benefit from antipsychotics, like Thorazine, still had 90% of their D2 dopamine receptors blocked. Conversely, it has been demonstrated that patients that did benefit from treatment had low levels of D2 blockade. In addition, the up-regulation of D2 receptors noted in post-mortem examination of schizophrenics’ brains could have been the result of the treatment they were on, not of the illness itself. Imaging of living, yet-untreated schizophrenics has not shown an increase in D2 receptors. It seems likely, then, that whatever the Thorazine is treating in my tour guide’s son was not schizophrenia. The mystery as to what the disorder actually is remains…but now I know why there is a mystery to begin with!